Furthermore, considering that long term potentiated synaptic transmission could be observed in the ACC after nerve injury and TBS induced LTP is occluded in animal model of neuropathic pain [15,30], our results also provide possible explanation for the occlusion of LTP in chronic pain conditions: the recruitment of GluA1 into synapses prevents any further AMPAR insertion triggered by LTP induction protocol. This evidence concerns the gene GRIA1 and injury.